6-bromo-3-(methoxycarbonylmethyl)benzenesulfonamide | 859232-73-8

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯和取代衍生物
• 英文名称: 6-bromo-3-(methoxycarbonylmethyl)benzenesulfonamide
• 英文别名: Methyl 2-(4-bromo-3-sulfamoylphenyl)acetate；methyl 2-(4-bromo-3-sulfamoylphenyl)acetate
• CAS: 859232-73-8
• 化学式: C₉H₁₀BrNO₄S
• 分子量: 308.153
• InChiKey: GNOZMASFUGEALQ-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  1
• 重原子数：
  16
• 可旋转键数：
  4
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.22
• 拓扑面积：
  94.8
• 氢给体数：
  1
• 氢受体数：
  5

反应信息

• 作为反应物：
  描述：

  6-bromo-3-(methoxycarbonylmethyl)benzenesulfonamide 在 四(三苯基膦)钯 吡啶 、 4-二甲氨基吡啶 、 sodium carbonate 作用下， 以 乙二醇二甲醚 为溶剂， 生成 N-acetyl-3-carboxymethyl-6-(4-methylthiophenyl)benzenesulfonamide
  参考文献：
  名称：

  Design, synthesis, and biological evaluation of N-acetyl-2-(or 3-)carboxymethylbenzenesulfonamides as cyclooxygenase isozyme inhibitors

  摘要：

  A group of N-acetyl-2-(or 3-)carboxymethylbenzenesulfonamides, possessing either a F or a substituted-phenyl ring substituent (4-F, 2,4-F,, 4-SO2Me, 4-OCHMe2) attached to its C-4 or C-6 position, was prepared using a palladium-catalyzed Suzuki cross-coupling reaction for evaluation as selective cyclooxygenase-2 (COX-2) inhibitors. Although N-acetyl-3-carboxymethyl-6-fluorobenzenesulfonamide [14, COX-1 IC50 = 2.26 mu M; COX-2 IC50 = 0.012 mu M; COX-2 selectivity index (SI) = 188] and N-acetyl-3-carboxymethyl-6-(4-isopropoxyphenyl)benzenesulfonamide (20c, COX-1 IC50 > 100 mu M; COX-2 IC50=0.15 mu M; COX-2 SI > 667) exhibited potent in vitro COX-2 inhibitory activity and high COX-2 selectivity, both compounds were inactive anti-inflammatory agents in a carrageenan-induced rat paw edema assay. In contrast, the less potent and less selective COX-2 inhibitors N-acetyl-2-carboxymethyl-4-fluorobenzenesulfonamide (12, COX-1 IC50 = 4.25 mu M; COX-2 IC50 = 0.978 mu M; COX-2 SI = 4.3), N-acetyl-2-carboxymethyl-4-(2,4-difluorophenyi)benzenesulfonamide (17c, COX-1 IC50 = 1.02 mu M; COX-2 IC50 = 1.00 mu M; COX-2 SI = 1.02), and N-acetyl-3-carboxymethyl-6-(4-methanesulfonylphenyl)benzenesulfonamide (20e, COX-1 IC50 = 0.109 mu M; COX-2 IC50 = 1.14 mu M; COX-2 SI = 0.095) exhibited moderate anti-inflammatory activity where a 75 mg/kg oral dose reduced inflammation 26%, 14%, and 20%, respectively, at 3 h postdrug administration relative to the reference drug aspirin where a 50 mg/kg oral dose reduced inflammation by 25% at 3 h postdrug administration. (c) 2005 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmc.2005.04.069
• 作为产物：
  描述：

  4-溴苯乙酸甲酯 在 氯磺酸 、 氨 作用下， 以 四氢呋喃 为溶剂， 反应 5.5h， 生成 6-bromo-3-(methoxycarbonylmethyl)benzenesulfonamide
  参考文献：
  名称：

  Design, synthesis, and biological evaluation of N-acetyl-2-(or 3-)carboxymethylbenzenesulfonamides as cyclooxygenase isozyme inhibitors

  摘要：

  A group of N-acetyl-2-(or 3-)carboxymethylbenzenesulfonamides, possessing either a F or a substituted-phenyl ring substituent (4-F, 2,4-F,, 4-SO2Me, 4-OCHMe2) attached to its C-4 or C-6 position, was prepared using a palladium-catalyzed Suzuki cross-coupling reaction for evaluation as selective cyclooxygenase-2 (COX-2) inhibitors. Although N-acetyl-3-carboxymethyl-6-fluorobenzenesulfonamide [14, COX-1 IC50 = 2.26 mu M; COX-2 IC50 = 0.012 mu M; COX-2 selectivity index (SI) = 188] and N-acetyl-3-carboxymethyl-6-(4-isopropoxyphenyl)benzenesulfonamide (20c, COX-1 IC50 > 100 mu M; COX-2 IC50=0.15 mu M; COX-2 SI > 667) exhibited potent in vitro COX-2 inhibitory activity and high COX-2 selectivity, both compounds were inactive anti-inflammatory agents in a carrageenan-induced rat paw edema assay. In contrast, the less potent and less selective COX-2 inhibitors N-acetyl-2-carboxymethyl-4-fluorobenzenesulfonamide (12, COX-1 IC50 = 4.25 mu M; COX-2 IC50 = 0.978 mu M; COX-2 SI = 4.3), N-acetyl-2-carboxymethyl-4-(2,4-difluorophenyi)benzenesulfonamide (17c, COX-1 IC50 = 1.02 mu M; COX-2 IC50 = 1.00 mu M; COX-2 SI = 1.02), and N-acetyl-3-carboxymethyl-6-(4-methanesulfonylphenyl)benzenesulfonamide (20e, COX-1 IC50 = 0.109 mu M; COX-2 IC50 = 1.14 mu M; COX-2 SI = 0.095) exhibited moderate anti-inflammatory activity where a 75 mg/kg oral dose reduced inflammation 26%, 14%, and 20%, respectively, at 3 h postdrug administration relative to the reference drug aspirin where a 50 mg/kg oral dose reduced inflammation by 25% at 3 h postdrug administration. (c) 2005 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmc.2005.04.069

文献信息

• Design, synthesis, and biological evaluation of N-acetyl-2-(or 3-)carboxymethylbenzenesulfonamides as cyclooxygenase isozyme inhibitors
  作者：Qiao-Hong Chen、P.N. Praveen Rao、Edward E. Knaus

  DOI：10.1016/j.bmc.2005.04.069

  日期：2005.8

  A group of N-acetyl-2-(or 3-)carboxymethylbenzenesulfonamides, possessing either a F or a substituted-phenyl ring substituent (4-F, 2,4-F,, 4-SO2Me, 4-OCHMe2) attached to its C-4 or C-6 position, was prepared using a palladium-catalyzed Suzuki cross-coupling reaction for evaluation as selective cyclooxygenase-2 (COX-2) inhibitors. Although N-acetyl-3-carboxymethyl-6-fluorobenzenesulfonamide [14, COX-1 IC50 = 2.26 mu M; COX-2 IC50 = 0.012 mu M; COX-2 selectivity index (SI) = 188] and N-acetyl-3-carboxymethyl-6-(4-isopropoxyphenyl)benzenesulfonamide (20c, COX-1 IC50 > 100 mu M; COX-2 IC50=0.15 mu M; COX-2 SI > 667) exhibited potent in vitro COX-2 inhibitory activity and high COX-2 selectivity, both compounds were inactive anti-inflammatory agents in a carrageenan-induced rat paw edema assay. In contrast, the less potent and less selective COX-2 inhibitors N-acetyl-2-carboxymethyl-4-fluorobenzenesulfonamide (12, COX-1 IC50 = 4.25 mu M; COX-2 IC50 = 0.978 mu M; COX-2 SI = 4.3), N-acetyl-2-carboxymethyl-4-(2,4-difluorophenyi)benzenesulfonamide (17c, COX-1 IC50 = 1.02 mu M; COX-2 IC50 = 1.00 mu M; COX-2 SI = 1.02), and N-acetyl-3-carboxymethyl-6-(4-methanesulfonylphenyl)benzenesulfonamide (20e, COX-1 IC50 = 0.109 mu M; COX-2 IC50 = 1.14 mu M; COX-2 SI = 0.095) exhibited moderate anti-inflammatory activity where a 75 mg/kg oral dose reduced inflammation 26%, 14%, and 20%, respectively, at 3 h postdrug administration relative to the reference drug aspirin where a 50 mg/kg oral dose reduced inflammation by 25% at 3 h postdrug administration. (c) 2005 Elsevier Ltd. All rights reserved.